Mutagens contribute to the human burden of heritable birth defects and cancer and probably to heart disease as well. Bacteriophage T4 has been widely employed as a model system to analyze mechanisms of mutagenesis. One of the most common T4 mutation assays recognizes r (rapid lysis) mutants by their large, sharply edged plaques. Although the rII mutants are those most often subjected to further analysis, most mutagens produce more rI than rII mutants. Since little is known about the rI mutants, we have investigated their general properties. Mutations that produce the characteristic rI phenotype arise at two loci, one the classically described locus at about 60 kb on the standard map and another a locus at about 1600 kb. Point mutations at the 60-kb locus recombine inter se at low frequencies, suggesting a small gene; several are suppressed by unlinked but as yet unmapped suppressor mutations. The 1600-kb locus is being cloned and more closely mapped.